Doctors Urge Adults To Get Tested For Lipoprotein(a), The ‘Sneaky’ Cholesterol Tied To Heart Risk Now

Cardiologists are urging adults to ask their doctors about a blood test that most people have never heard of, one that measures a genetically inherited form of cholesterol linked to heart attacks and strokes but left off the standard lipid panel most patients receive at routine checkups.

The substance, known as lipoprotein(a), or Lp(a), is a distinct cholesterol particle that circulates in the bloodstream and functions as a major independent risk factor for cardiovascular disease, according to Ryan Smith, a cardiologist at Orlando Health Heart and Vascular Institute. Unlike LDL cholesterol, HDL cholesterol and triglycerides, the three markers typically included in a standard lipid panel, Lp(a) is not part of routine bloodwork, meaning many people go years, or a lifetime, without knowing their level.

That gap in testing has drawn increasing attention from the medical community. In March, a coalition of medical organizations, including the American Heart Association, released updated cholesterol management guidelines recommending, for the first time, that every adult be tested for Lp(a) at least once in their lifetime. The test can be ordered by a primary care physician as an addition to a standard lipid profile or other routine bloodwork, and it is now largely covered by major insurance plans, removing what had previously been a financial barrier for many patients.

Roughly one in five people have an elevated Lp(a) level, according to figures cited by cardiologists, and like other forms of high cholesterol, it typically produces no symptoms until it contributes to a blockage that triggers a heart attack or stroke. An Lp(a) level above 125 nanomoles per liter, sometimes measured as 50 milligrams per deciliter, has been shown to raise the risk of heart disease and stroke, with that risk potentially doubling at levels around 250 nanomoles per liter, or 100 milligrams per deciliter.

Lp(a) poses a particular danger because of its molecular structure. Much like excess LDL cholesterol, elevated Lp(a) can accumulate in the arteries and contribute to atherosclerosis, a narrowing of blood vessels that restricts blood flow to vital organs. But because Lp(a) carries an additional protein component called apolipoprotein A, it tends to be stickier and more prone to forming fatty plaques than LDL cholesterol, according to Smith. The particle can also interfere with the body’s natural clot-breakdown process, potentially increasing the likelihood of blood clots, and it carries pro-inflammatory molecules that can damage the aortic valve and contribute to arterial hardening over time.

For decades, Lp(a) testing was left out of standard cholesterol guidance largely because there was little clarity on what patients or doctors could actually do about an elevated result, according to Jeffrey Berger, director of the Center for the Prevention of Cardiovascular Disease at NYU Langone Heart. Researchers still do not know definitively whether lowering Lp(a) levels reduces cardiovascular risk, though Berger said ongoing research and drug trials increasingly point toward that possibility. Because Lp(a) levels are driven almost entirely by genetics, they generally do not respond to the lifestyle changes, such as diet and exercise, that can meaningfully lower other types of cholesterol.

Even without a clear treatment pathway, physicians say the case for testing has become increasingly clear. Berger said a growing body of evidence has repeatedly shown how elevated Lp(a) raises the likelihood of a cardiac event, making it important for patients to know whether they carry the genetic risk factor so they can more aggressively manage the cardiovascular risks that are modifiable.

Certain populations face a higher likelihood of elevated Lp(a) levels, given the trait’s strong genetic basis. People of African or South Asian descent tend to show the highest rates, followed by white, Hispanic and East Asian populations, according to cardiologists. The American Heart Association specifically recommends testing for anyone with a family history of high Lp(a), a personal or family history of early cardiovascular disease, defined as before age 55 in men and before 65 in women, and those with familial hypercholesterolemia, an inherited condition that causes elevated LDL levels.

For most people, a single Lp(a) test provides a reliable, lifelong measure of risk, since the level typically remains stable over time, Smith said. Exceptions include people with thyroid disorders, a kidney condition called nephrotic syndrome, certain acute inflammatory conditions, and those who are pregnant or in menopause, all of which can temporarily elevate Lp(a) readings. Once those conditions resolve or are treated, Lp(a) levels generally return to their genetic baseline.

Because no treatments currently exist that meaningfully lower Lp(a) on their own, doctors recommend that people with elevated levels focus on aggressively managing other cardiovascular risk factors, particularly blood pressure, blood sugar and LDL cholesterol. Research suggests that lowering LDL by an additional 20 milligrams per deciliter or more below the standard target of 100 milligrams per deciliter can help offset some of the added risk associated with high Lp(a). The American Heart Association recommends at least 150 minutes of moderate-intensity physical activity per week, a diet rich in plant-based foods, avoiding smoking, maintaining a healthy weight, and getting seven to nine hours of sleep nightly as foundational steps for cholesterol management.

Patients with high Lp(a) are often prescribed statins to more aggressively lower LDL cholesterol, and some physicians may add ezetimibe, a non-statin medication that blocks cholesterol absorption in the small intestine and can modestly reduce Lp(a) as well. Others may prescribe a PCSK-9 inhibitor, a class of drug that helps the liver clear LDL cholesterol from the blood and may offer a modest reduction in Lp(a) levels; a newly approved oral version of the drug has shown efficacy comparable to the injectable PCSK-9 inhibitors already available.

Looking ahead, a new class of medications currently in late-stage clinical trials is designed to directly target the RNA responsible for producing lipoprotein(a) in the body. Early data suggests these drugs can meaningfully lower Lp(a) levels, though it remains unclear whether that reduction will translate into fewer heart attacks and strokes.

For now, physicians say the priority is simply raising awareness of the test itself. Smith said Lp(a) should be viewed as one piece of a broader conversation with a doctor about overall cardiovascular risk, one best raised as early as possible. “Prevention is really supreme in our field,” he said.